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DEN 2026 - Pharmacology > Antiplatelet Agents > Flashcards

Antiplatelet Agents Flashcards

(40 cards)

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1
Q

What is haemostasis?

A

Arrest of haemorrhage

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2
Q

What is thrombosis?

A

Pathological formation of a haemostatic plug within the vasculature in the absence of bleeding

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3
Q

Name 3 processes involved in haemostasis

A
  1. Vessel wall constriction
  2. Platelet adhesion to sub-endothelial collagen, degranulation, aggregation and plug formation
  3. Blood coagulation
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4
Q

What is Virchow’s Triad?

A

Three broad categories of factors that contribute to thrombosis

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5
Q

What are the 3 categories which make up Virchow’s Tried?

A
  1. Stasis of blood flow
  2. Endothelial injury
  3. Hypercoagulability
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6
Q

Name 3 types of anti-platelet agents

A
  1. Cyclo-oxygenase inhibitors
  2. ADP receptor pathway inhibitors
  3. Phosphodiesterase inhibitors
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7
Q

What is the function of anti-platelet drugs?

A

Decrease platelet aggregation and inhibit thrombus formation in the arterial circulation

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8
Q

What do anti-platelet drugs work on the arterial circulation?

A

In fast-flowing vessels thrombi are composed of platelets with little fibrin

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9
Q

What 3 substances released by platelets promote aggregation?

A
  1. ADP
  2. Thromboxane A2 (TXA2)
  3. Serotonin (5-HT)
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10
Q

What substance released by the endothelium inhibits platelet aggregation?

A

Prostaglandin I2 (PGI2)

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11
Q

Name the 3 pathways of coagulation?

A
  1. Extrinsic
  2. Intrinsic
  3. Common
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12
Q

How is the formation of PGH2 catalysed?

A

COX-1 and COX-2 enzymes

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13
Q

What happens to PGH2 in the blood vessel walls?

A

Converted to PGI2 in wall

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14
Q

What happens to PGH2 in platelets?

A

Converted to TXA2

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15
Q

What is the mechanism of action of aspirin as an anti-platelet?

A

Selective and irreversible inactivation of COX-1 enzymes by acetylation of serine residue

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16
Q

Why is it desirable for aspirin to inactivate COX-1 enzymes?

A

COX-1 enzymes catalyse production of PGH2 from arachidonic acid so TXA2 cannot form to cause aggregation

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17
Q

What dose of aspirin is used to provide anti-platelet function?

18
Q

Why does platelet function recover if aspirin is stopped, even though it is non-reversible?

Study These Flashcards
A
  • Platelet lifespan is 7-10 days
  • New platelets are released often
  • New platelets are not inactivated
19
Q

Why can inhibited platelets not regenerate new COX-1 enzymes?

Study These Flashcards
A

There is no nuclei present in platelet cells

20
Q

Describe 5 clinical indications for prescribing aspirin at low doses as secondary prevention measures

Study These Flashcards
A
  1. Ischaemic stroke
  2. Acute coronary syndrome
  3. Post myocardial infarction
  4. Angina pectoris
  5. Atrial fibrillation
21
Q

Name 3 adverse effects of aspirin

Study These Flashcards
A
  1. GI irritation
  2. Hypersensitivity reactions
  3. Reye’s syndrome in children
22
Q

How may gastric irritation be reduced in a patient taking aspirin?

Study These Flashcards
A

Co-administration of acid suppressant drugs

23
Q

Name 4 interactions of aspirin

Study These Flashcards
A
  1. NSAIDs
  2. Corticosteroids
  3. Anticoagulants
  4. Other anti-platelet agents
24
Q

How does ADP influence platelet function?

Study These Flashcards
A
  • ADP binds to purinergic P2Y12 receptors on platelets
  • Unmasks glycoprotein GPIIb/IIIa receptors
  • Exposed to fibrinogen
  • Enhanced aggregation
25
Give the main type of ADP receptor pathway inhibitors drug and two examples of this type
Thienopyridines (clopidogrel and prasugrel)
26
How do thienopyridines function?
Selectively and irreversibly inhibit ADP-mediated platelet activation and aggregation
27
Describe the mechanism of action of clopidogrel
- Pro-drug administered orally - 85% hydrolysed by esterases after absorption - 15% undergoes 2-step oxidation in liver by CYP2C19 enzymes - Active metabolite selective and irreversible inhibitor of ADP-dependent platelet activation
28
What are 2 clinical indications for clopidogrel?
1. Secondary prevention in patients intolerant of aspirin 2. With aspirin for 3-12 months after acute coronary syndrome and following procedures to coronary arteries to prevent thrombosis
29
Name 3 adverse affects of clopidogrel
1. GI irritation and bleeding 2. Dyspepsia 3. Hypersensitivity reactions
30
When may clopidogrel cause the most GI irritation and bleeding?
When being co-administered with clopidogrel
31
What are 4 potential drawbacks of clopidogrel?
- Pro-drug means there is delayed onset of action - Genetic variation of liver enzymes responsible for metabolism so response varies between patient - Drug-drug interactions - Irreversible inhibition of P2Y12 receptor
32
Name a drug-drug interaction of clopidogrel
Proton pump inhibitors influence liver enzymes which metabolise clopidogrel
33
Why does prasugrel tend to be more potent and predictable than clopidogrel?
- There is less dependence on enzymes in the liver to form the active metabolite as the oxidation is a one-step process - Metabolites form in a more consistent fashion, in higher concentrations
34
When is prasugrel used?
Acute coronary syndrome in short term as there is a greatly increased risk of bleeding
35
How does ticagrelor inhibit ADP receptor pathways?
- Inhibitory allosteric modulator of P2Y12 receptor | - Inhibits G-protein signalling
36
What are 3 mechanisms of dipyridamole?
- Thromboxane synthase inhibitor [THA2 decreases] - Phosphodiesterase inhibitor [cAMP increases] - Inhibition of reuptake and metabolism of adenosine
37
What is the use of increasing cAMP concentration?
Less platelets are active
38
What is the use of decreasing reuptake and metabolism of adenosine?
Adenosine has a vasodilatory effect and inhibits platelet activity so reduced uptake reduces clearance rate
39
What are 2 clinical indications of dipyridamole?
1. Co-administration with aspirin for secondary prevention of ischaemic stroke 2. Co-administration with oral anticoagulants for prevention of thromboembolism in patients with prosthetic heart valves
40
Name 3 adverse effects of dipyridamole
1. GI irritation and bleeding 2. Dizziness / flushing 3. Hypersensitivity reactions

DEN 2026 - Pharmacology (22 decks)

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